Is avascular necrosis of the femoral head the result of inhibition of angiogenesis?
An hypothesis is offered here that the pathogenesis of avascular necrosis (AVN) of the femoral head is based on the inhibition of angiogenesis. Well-established facts supporting this hypothesis are: 1, the lesion of AVN is vascular obliteration often leading to infarction; 2, glucocorticoids, which are a risk factor for AVN, are inhibitors of angiogenesis; 3, interferons, which are now being used in the treatment of multiple sclerosis, hepatitis, leukemias, and hemangiomas are inhibitors of angiogenesis, and other endogenously produced cytokines are also inhibitors; 4, constituents of cartilage are inhibitors of angiogenesis, explaining the subchondral location of AVN; 5, angiography of the femoral head indicates the need for continual renewal of its blood supply, shows the inhibition of revascularization by steroids, and suggests that the stress of weight bearing makes the femoral head particularly vulnerable. This hypothesis has implications for the therapeutic use of inhibitors of angiogenesis.
Smith
D W
DW
Department of Pathology and Buehler Center on Aging, Northwestern University School of Medicine, Chicago, IL 60611-2611, USA.
D000818:Animals; D005270:Femur Head / Q000098:blood supply; D005271:Femur Head Necrosis / Q000209:etiology / Q000503:physiopathology*; D005938:Glucocorticoids / Q000009:adverse effects; D006801:Humans; D007238:Infarction; D007372:Interferons / Q000009:adverse effects; D008954:Models, Biological; D018919:Neovascularization, Physiologic; D012307:Risk Factors
D005938:Glucocorticoids; D007372:Interferons